Aging is associated with a decline in muscle mass and strength, called sarcopenia, which is an important cause of frailty and disability in the elderly. There is a decline in both the number and size of muscle fibers with age which contributes to the weakness seen in aging skeletal muscle. However, functional alterations at the muscle cell level with sarcopenia have not been studied thoroughly. The only intervention proven to reverse the weakness caused by sarcopenia to date is progressive resistance training (PRT). No reports have examined the relative contribution of changes in single fiber contractility (i.e., muscle quality) versus muscle mass (i.e., muscle quantity) in the etiology or treatment of sarcopenia. In this exploratory grant, we propose to assess for the first time changes in the contractile properties of single muscle fibers with age, and their response to PRT in sarcopenic elderly women. They hypothesize that aging is associated with a decrease in the maximal force, specific force (force/area), and shortening velocity of type I and IIA muscle fibers; that maximal and specific force production by single muscle fibers correlates with in vivo measurements of muscle strength in young and elderly subject; and that PRT will stimulate gains in specific force production in single fibers as well as in vivo. They propose to recruit 8 young healthy sedentary women (ages 18-30) and 16 elderly, healthy women (ages 70-85) and evaluate the strength, in vivo muscle CSA by CT scan, and specific force of their quadriceps femoris muscle group. The elderly women will then be randomly assigned to strength training (n = 8) or control activity (n = 8) for 12 weeks. These data will be used as the basis for subsequent studies examining the relationship between muscle fiber quality and functional status of elderly adults with sarcopenia. In addition, these methods will allow assessment of muscle cell function independently of central nervous system influence, setting the stage for future studies to better define the role of peripheral versus central mechanisms in the etiology and treatment of sarcopenia.